ArticleCell cycle (Georgetown, Tex.)2016
Bim directly antagonizes Bcl-xl in doxorubicin-induced prostate cancer cell apoptosis independently of p53.
Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Meta analysis of bioactive compounds, miRNA, siRNA and cell death regulators as sensitizers to doxorubicin induced chemoresistance.Apoptosis : an international journal on programmed cell death · 2022Pooled it
- A unified therapeutic theory for treating cancer via master regulators of the universal apoptosis network.Cell death discovery · 2026Review
- Protease-activated receptor 2 attenuates doxorubicin-induced apoptosis in colon cancer cells.Journal of cell communication and signaling · 2023Article
- Triple negative breast cancer: approved treatment options and their mechanisms of action.Journal of cancer research and clinical oncology · 2023Article
- Regorafenib induces Bim-mediated intrinsic apoptosis by blocking AKT-mediated FOXO3a nuclear export.Cell death discovery · 2023Article
- SIRT1 inhibition-induced senescence as a strategy to prevent prostate cancer progression.Molecular carcinogenesis · 2022Article
- Severe cellular stress drives apoptosis through a dual control mechanism independently of p53.Cell death discovery · 2022Review
- Compound cellular stress maximizes apoptosis independently of p53 in glioblastoma.Cell cycle (Georgetown, Tex.) · 2022Article
- Akt inhibitor augments anti-proliferative efficacy of a dual mTORC1/2 inhibitor by FOXO3a activation in p53 mutated hepatocarcinoma cells.Cell death & disease · 2021Article
- Caryophyllene Oxide, the Active Compound Isolated from Leaves ofMolecules (Basel, Switzerland) · 2021Article
- Severe cellular stress activates apoptosis independently of p53 in osteosarcoma.Cell death discovery · 2021Article
- MUC1 is an oncoprotein with a significant role in apoptosis (Review).International journal of oncology · 2021Review
- Review
- Downregulation of ATXN3 Enhances the Sensitivity to AKT Inhibitors (Perifosine or MK-2206), but Decreases the Sensitivity to Chemotherapeutic Drugs (Etoposide or Cisplatin) in Neuroblastoma Cells.Frontiers in oncology · 2021Article
- EGCG Enhanced the Anti-tumor Effect of Doxorubicine in Bladder Cancer via NF-κB/MDM2/p53 Pathway.Frontiers in cell and developmental biology · 2020Article
- BCL-2 Inhibitor Venetoclax Induces Autophagy-Associated Cell Death, Cell Cycle Arrest, and Apoptosis in Human Breast Cancer Cells.OncoTargets and therapy · 2020Article
- miRNA-29b Inhibits Prostate Tumor Growth and Induces Apoptosis by Increasing Bim Expression.Cells · 2019Article
- Topological properties and in vitro identification of essential nodes of the Paclitaxel and Vincristine interactomes in PC-3 cells.Biomedical journal · 2019Article
- Transcription-independent and -dependent p53-mediated apoptosis in response to genotoxic and non-genotoxic stress.Cell death discovery · 2019Article
- Epigenetic silencing of TMEM176A activates ERK signaling in human hepatocellular carcinoma.Clinical epigenetics · 2018Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Doxorubicin and other anthracycline compounds exert their anti-cancer effects by causing DNA damage and initiating cell cycle arrest in cancer cells, followed by apoptosis. DNA damage generally activates a p53-mediated pathway to initiate apoptosis by increasing the level of the BH3-only protein, Puma. However, p53-mediated apoptosis in response to DNA damage has not yet been validated in prostate cancers. In the current study, we used LNCaP and PC3 prostate cancer cells, representing wild type p53 and a p53-null model, to determine if DNA damage activates p53-mediated apoptosis in prostate cancers. Our results revealed that PC3 cells were 4 to 8-fold less sensitive than LNCaP cells to doxorubicin-inuced apoptosis. We proved that the differential response of LNCaP and PC3 to doxorubicin was p53-independent by introducing wild-type or dominant negative p53 into PC3 or LNCaP cells, respectively. By comparing several apoptosis-related proteins in both cell lines, we found that Bcl-xl proteins were much more abundant in PC3 cells than in LNCaP cells. We further demonstrated that Bcl-xl protects LNCaP and PC3 cells from doxorubicin-induced apoptosis by using ABT-263, an inhibitor of Bcl-xl, as a single agent or in combination with doxorubicin to treat LNCaP or PC3 cells. Bcl-xl rather than p53, likely contributes to the differential response of LNCaP and PC3 to doxorubicin in apoptosis. Finally, co-immunoprecipitation and siRNA analysis revealed that a BH3-only protein, Bim, is involved in doxorubicin-induced apoptosis by directly counteracting Bcl-xl.
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